Sensory nerve regeneration after epithelium wounding in normal and diabetic cornea

Abstract

The cornea is the most densely innervated mammalian tissue. The sensory nerves are responsible for sensations of dryness, temperature, touch, and pain, and play important roles in the blink reflex, wound healing, and tear production. Many ocular and systemic diseases can adversely affect corneal sensory nerve and consequently impair their function. One of such systemic diseases is diabetes mellitus (DM) which causes sensory degeneration, neurotrophic keratopathy (DNK), and delayed wound healing. In this review, we summarize recent discoveries revealing mechanisms underlying the pathogenesis of DNK and the impairment of sensory nerve regeneration in post wound diabetic corneas in using animal model of human diabetes. Because it is generally believed that common mechanisms are operative in the pathogenesis of diabetic peripheral neuropathy in different tissues, the findings in the corneas have implications in in other tissues such as the skin, which often leads to foot ulceration and amputation in diabetic patients.

Figure 1

Defects of corneal innervations in 1-month-old GK rats. Subbasal plexus of the central cornea of Wistar and type 2 diabetes Goto-Kakizaki (GK) rat was visualized with Whole-mount immunostaining of β-tubulin and representative images are shown.